Modulation of the composition of AP-1 complex and its impact on transcriptional activity

Acta Neurobiologiae Experimentalis

Volumn 60, Issue 3, 2000, Pages 395-402

  Kaminska, B ^a   Pyrzynska, B ^a   Ciechomska, I ^a   Wisniewska, M ^a  

^a NENCKI INSTITUTE OF EXPERIMENTAL BIOLOGY   (Poland)

Author keywords

ATF 2; c Jun protein; Jun proteins; Long term responses; Neurodegeneration; Protein phosphorylation; Transcription factors

Indexed keywords

TRANSCRIPTION FACTOR AP 1;

CELL ACTIVATION; CELL PROLIFERATION; CONFERENCE PAPER; GENETIC TRANSCRIPTION; NERVE CELL; NONHUMAN; PROTEIN ANALYSIS; PROTEIN DNA BINDING; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION;

ANIMALS; HUMANS; PHOSPHORYLATION; SIGNAL TRANSDUCTION; TRANSCRIPTION FACTOR AP-1;

EID: 0033838974     PISSN: 00651400     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Conference Paper

References (59)

1. Transcriptional regulation by Fos and Jun in vitro: Interaction among multiple activator and regulatory domains
2. The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation
3. Heterodimer formation between CREB and JUN proteins
4. Induction of apoptosis by the transcription factor c-Jun
5. Expression and involvement of c-fos and c-jun protooncogenes in programmed cell death induced by growth factor deprivation in lymphoid cell lines
6. Fos: An immediate-early transcription factor in neurons
7. JunB differs from c-Jun in its DNA-binding and dimerization domains, and represses c-Jun by formation of inactive heterodimers
8. JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain
9. The role of inducible transcription factors in apoptotic nerve cell death
10. Role of the Jun kinase pathway in the regulation of c-Jun expression and apoptosis in sympathetic neurons
11. Altered gene expression in neurons during programmed cell death: Identification of c-jun as necessary for neuronal apoptosis
12. Light-induced variations in AP-1 binding activity and composition in the rat suprachiasmatic nucleus
13. In vitro association between the Jun protein family and the general transcription factors, TBP and TFIIB
14. Transcription factor ATF2 regulation by the JNK signal transduction pathway
15. Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity
16. c-Jun dimerizes with itself and with c-Fos, forming complexes of different DNA binding affinities
17. A c-Jun dominant negative mutant protects sympathetic neurons against programmed cell death
18. Essential role of the fosB gene in molecular, cellular, and behavioral actions of chronic electroconvulsive seizures
19. Lasting N-terminal phosphorylation of c-Jun and activation of c-Jun N-terminal kinases after neuronal injury
20. Inducible and constitutive transcription factors in the mammalian nervous system: Control of gene expression by Jun, Fos and Krox, and CREB/ATF proteins
21. The c-Jun transcription factor-bipotential mediator of neuronal death, survival and regeneration
22. Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain
23. Chronic electroconvulsive seizure (ECS) treatment results in expression of a long-lasting AP-1 complex in brain with altered composition and characteristics
24. Activity and injury-dependent expression of inducible transcription factors, growth factors and apoptosis-related genes within the central nervous system
25. Sensory regulation of immediate-early gene expression in mammalian visual cortex: Implications for functional mapping and neural plasticity
26. c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions
27. Dynamic changes in the composition of the AP-1 transcription factor DNA-binding activity in rat brain following kainate-induced seizures and cell death
28. Visual stimulation regulates the expression of transcription factors and modulates the composition of AP-1 in visual cortex
29. Rapid phosphorylation of Elk-1 transcription factor and activation of MAP kinase signal transduction pathways in response to visual stimulation
30. Elevated AP-1 transcription factor DNA binding activity at the onset of functional plasticity during development of rat sensory cortical areas
31. The regulation of AP-1 activity by mitogen-activated proetin kinases
32. AP-1 function and regulation
33. DNA damaging agents induce expression of Fas ligand and subsequent apoptosis in T lymphocytes via the activation of NF-kappa B and AP-1
34. Kainic acid-induced neuronal death is associated with DNA damage and a unique immediate-early gene response in c-fos-lacZ transgenic rats
35. Existence of different Fos/Jun complexes during the G0-to-G1 transition and during exponential growth in mouse fibroblasts: Differential role of Fos proteins
36. Variations in Jun and Fos protein expression and AP-1 activity in cycling, resting and stimulated fibroblasts
37. Withdrawal of survival factors results in activation of the JNK pathway in neuronal cells leading to Fas ligand induction and cell death
38. AP-1 and CRE DNA binding activities in rat brain following pentylenetetrazole induced seizures
39. Defensive conditioning-related increase in AP-1 transcription factor in the rat cortex
40. CD95 ligand (Fas-L/APO-1L) and tumor necrosis factor-related apoptosis-inducing ligand mediate ischemia-induced apoptosis in neurons
41. c-Jun N-terminal phosphorylation correlates with activation of the JNK subgroup but not the ERK subgroup of mitogen-activated protein kinases
42. Immediate-early genes: Ten years on
43. Cyclosporin A, an immuno- suppressive drug, induces programmed cell death in rat C6 glioma cells by a mechanism that involves the AP-1 transcription factor
44. Nuclear factor of activated T cells (NFAT) as a new component of the signal transduction pathway in glioma cells
45. DeltaFosB: A molecular mediator of long-term neural and behavioral plasticity
46. AP-1 transcription factors: Short- and long-term modulators of gene expression in the brain
47. Kainate-induces changes in opioid peptide gene and AP-1 protein expression in the rat hippo-campus
48. The stress-activated protein kinases are major c-Jun amino-terminal kinases activated by-ischemia and reperfusion
49. Phosphorylation of c-jun mediated by MAP kinases
50. Changes of the trans-activating potential of AP-1 transcription factor during cyclosporin A-induced apoptosis of glioma cells are mediated by phosphorylation and alterations of AP-1 composition
51. Differentiation of mouse keratinocytes is accompanied by PKC-dependent changes in AP-1 proteins
52. Opposing activities of c-Fos and Fra-2 on AP-1 regulated transcriptional activity in mouse keratinocytes induced to differentiate by calcium and phorbol esters
53. c-JUN, JUN B, and JUN D differ in their binding affinities to AP-1 and CRE consensus sequences: Effect of FOS proteins
54. Dynamic alterations occur in the levels and composition of transcription factor AP-1 complexes after seizure
55. Compositional changes of AP-1 DNA-binding proteins are regulated by light in a mammalian circadian clock
56. Phosphorylation of c-Jun is necessary for apoptosis induced by survival signal withdrawal in cerebellar granule neurons
57. c-Jun regulates cell cycle progression and apoptosis by distinct mechanisms
58. Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis
59. Antitumor promotion by phenolic antioxidants: Inhibition of AP-1 activity through induction of Fra expression